TY - JOUR
T1 - Induction of apoptosis of malignant gliomas cells by a prenylated chalcone
AU - Teng, Chih Chuan
AU - Sze, Chun I.
AU - Liao, Wayne C.
N1 - Publisher Copyright:
© 2014 Informa Healthcare USA, Inc. All rights reserved.
PY - 2014/4/1
Y1 - 2014/4/1
N2 - Context: Malignant gliomas are the most commonly diagnosed brain tumors in adults. Chalcone and its derivatives have shown potential against glioblastoma and malignant gliomas. Objective: The inhibitory activity of geranyl prenylated chalcone was investigated in four glioma cell lines: C6, U87 MB, CNS-1 and 13-06 MB. Cell death caused by the prenylated chalcone was determined to be necrosis or apoptosis. Materials and methods: The inhibitory activity of geranyl prenylated chalcone with 5, 10, 15, 20, 25, 30 and 40 μg/ml (treatment time: 24, 48 and 72 h) was investigated in C6, U87 MB, CNS-1 and 13-06 MB. Cell cycle distribution, DNA fragmentation, chromatin condensation and protein expression were used as indicators of apoptosis. The migration ability of glioma cells with 30 μg/ml prenylated chalcone after 24 and 36 h incubation was also studied by the scratch wound assay. Results: After 24 h, treatment with 20 μg/ml prenylated chalcone reduced the proliferation (approximately 50%) of all four glioma cell lines (half maximal inhibitory concentration (IC50) = 20 μg/ml). Glioma cell death was verified by the fluorescence-activated cell sorter as prenylated chalcone-induced apoptosis. After running the analysis of protein expression, apoptotic activity induced by the prenylated chalcone was caspase independent for the C6 and U87 MB cell lines, but caspase dependent for the 13-06 MB and CNS-1 cell lines. In addition, prenylated chalcone treatment (30 μg/ml) resulted in the inhibition of glioma cell migration after 24 and 36 h treatment. Discussion and conclusion: Because prenylated chalcone-induced apoptosis inhibited the proliferation and reduced the invasiveness of glioma cells, the prenylated chalcone has potential as a new chemotherapeutic reagent in the treatment of malignant gliomas. The ultimate goal was to develop a novel potential multi-therapy for treating gliomas.
AB - Context: Malignant gliomas are the most commonly diagnosed brain tumors in adults. Chalcone and its derivatives have shown potential against glioblastoma and malignant gliomas. Objective: The inhibitory activity of geranyl prenylated chalcone was investigated in four glioma cell lines: C6, U87 MB, CNS-1 and 13-06 MB. Cell death caused by the prenylated chalcone was determined to be necrosis or apoptosis. Materials and methods: The inhibitory activity of geranyl prenylated chalcone with 5, 10, 15, 20, 25, 30 and 40 μg/ml (treatment time: 24, 48 and 72 h) was investigated in C6, U87 MB, CNS-1 and 13-06 MB. Cell cycle distribution, DNA fragmentation, chromatin condensation and protein expression were used as indicators of apoptosis. The migration ability of glioma cells with 30 μg/ml prenylated chalcone after 24 and 36 h incubation was also studied by the scratch wound assay. Results: After 24 h, treatment with 20 μg/ml prenylated chalcone reduced the proliferation (approximately 50%) of all four glioma cell lines (half maximal inhibitory concentration (IC50) = 20 μg/ml). Glioma cell death was verified by the fluorescence-activated cell sorter as prenylated chalcone-induced apoptosis. After running the analysis of protein expression, apoptotic activity induced by the prenylated chalcone was caspase independent for the C6 and U87 MB cell lines, but caspase dependent for the 13-06 MB and CNS-1 cell lines. In addition, prenylated chalcone treatment (30 μg/ml) resulted in the inhibition of glioma cell migration after 24 and 36 h treatment. Discussion and conclusion: Because prenylated chalcone-induced apoptosis inhibited the proliferation and reduced the invasiveness of glioma cells, the prenylated chalcone has potential as a new chemotherapeutic reagent in the treatment of malignant gliomas. The ultimate goal was to develop a novel potential multi-therapy for treating gliomas.
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U2 - 10.3109/13880209.2013.843573
DO - 10.3109/13880209.2013.843573
M3 - Article
AN - SCOPUS:84925258275
SN - 1388-0209
VL - 52
SP - 471
EP - 478
JO - Pharmaceutical Biology
JF - Pharmaceutical Biology
IS - 4
ER -